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Conclusion: These results suggest that LDL lipid peroxides play a role in modulating and attenuating platelet aggregation during strenuous exercise.

It has been suggested that regular physical activity prevents ischemic heart disease (21,28). However, exercise enhances oxygen consumption, resulting in oxygen-related free radical generation and oxidative stress, which are linked to membrane damage, lipid peroxidation, and platelet activation (9,22,32). Low-density lipoprotein (LDL) is reported to activate platelet functions, such as enhancement of thromboxane (TX) release and induction of platelet aggregation (41,45,48), and to be modified under oxidative stress such as exercise (19,20). Recently, it has been reported that the platelet-activating function of LDL resides more in the modified forms of LDL than in native LDL (23,46). Because both forms of LDL are major risk factors for cardiovascular disease, their interactions with platelets, therefore, may play an important role in the pathogenesis of atherosclerosis (25,39).

No reports have appeared on the combined effect of exercise and LDL (native or modified) on platelet-activating activities, such as TX release and platelet aggregation. Oldroyd et al. (31) reported that plasma lipid peroxide activity and TX production can be simultaneously increased under oxidative stress. In a previous study, we observed that the levels of LDL lipid peroxides seen during atrial pacing-induced ischemia correlated with myocardial ischemia and TX release (20). The purpose of this study was therefore to investigate the interaction between strenuous exercise and LDL, as well as their effects on platelet activity. We also attempted to determine whether lipid peroxides in plasma or LDL are a contributing factor for platelet activity during exercise.

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